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  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Regulatory Peptides 14 (1986), S. 33-39 
    ISSN: 0167-0115
    Keywords: gastrin ; parietal cells ; rat ; somatostatin ; starvation ; stomach
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 8 (1972), S. 250-259 
    ISSN: 1432-0428
    Keywords: Insulinoma ; immunohistologic investigation of B-cell tumours ; peroxidase labelled antibodies ; insulin and C-peptide in B-cells ; insulin concentration of insulinomas ; difference between insulin in normal and tumour B-cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Résumé 14 insulinomes ont été soumis à un examen immunohistologique à l'aide de la méthode de l'anticorps marqué à la peroxydase. 8 tumeurs ont été étudiées immédiatement après leur extirpation. 7 d'entre elles réagissaient avec les sérums anti-insuline et anti-porcine-C-peptide, mais non avec le sérum anti-glucagon. Un seul carcinome à cellules B avec un contenu en insuline inhabituellement bas, a été négatif. Un an après l'inclusion dans la paraffine, la réaction immunohistologique avec le sérum anti-insuline avait nettement diminué dans les tumeurs, mais non dans les îlots du pancréas adjacent. Chez 6 patients, on disposait de fragments de la tumeur et du pancréas normal inclus dans la paraffine depuis 1 à 4 ans. Dans ce groupe, 4 tumeurs avec un contenu élevé en insuline, n'avaient qu'une faible réaction immunohistologique avec un sérum antiinsuline, et deux tumeurs (l'une avec un contenu élevé en insuline, l'autre avec un contenu faible) ont eu une réaction immunohistologique négative, tandis que les îlots du pancréas adjacent réagissaient fortement dans les six cas. Donc, la réaction immunohistologique de l'insuline dans les tumeurs à cellules B, mais non dans les îlots normaux, dépend du temps écoulé entre l'inclusion dans la paraffine et le moment où elles sont examinées. Seules les tumeurs fixées dans du liquide de Bouin, mais non dans la solution de Karnovsky, ont eu une réaction immunohistologique positive, tandis que les îlots du pancréas adjacent réagissaient positivement après fixation dans la solution de Karnovsky. Ces résultats suggèrent qu'il existe des différences entre l'insuline du pancréas normal et l'insuline des tumeurs. Une comparaison entre la coloration à l'aldéhyde-thionine et l'immunohistologie indique la supériorité de l'immunohistologie dans l'identification des cellules tumorales produisant de l'insuline.
    Abstract: Zusammenfassung 14 insulinproduzierende Tumoren wurden mittels Peroxydase-markierter Antikörper immunhistologisch untersucht. 8 Tumoren gelangten unmittelbar postoperativ zur Untersuchung. Hiervon ließen sich 7 mit einem Antiserum gegen Insulin und Schweine-C-Peptid, nicht aber mit einem Antiserum gegen Glucagon anfärben. Dagegen reagierte ein B-Zellcarcinom mit einer sehr niedrigen Insulinkonzentration mit keinem dieser Seren. Bereits ein Jahr nach der Einbettung in Paraffin ließ die Anfärbbarkeit dieser Tumoren mit einem Antiinsulinserum deutlich nach, während die Inseln des umgebenden normalen Pankreas mit dem gleichen Serum unverändert stark reagierten. — Von 6 weiteren Inseladenomen standen außerdem 1– 4 Jahre altes paraffineingebettetes Tumor- und Pankreasgewebe zur Verfügung. 4 dieser Tumoren hatten eine erhöhte Insulinkonzentration, reagierten immunhistologisch jedoch mit einem Antiinsulinserum nur schwach. Die beiden restlichen Tumoren — einer mit einer hohen, der andere mit einer niedrigen Insulinkonzentration — verhielten sich immunhistologisch negativ. Im Gegensatz zu den Tumoren ließen sich die Inseln des umgebenden Pankreas sämtlicher 6 Fälle mit einem Insulinantiserum gut anfärben. Somit scheint der erfolgreiche immunhistologische Nachweis von Insulin in insulinproduzierenden Tumoren von der Dauer der Einbettung des Tumormaterials in Paraffin abzuhängen. Das Insulin in den Pankreasinseln unterliegt dagegen diesem „Alterungseffekt“ nicht. — TumorInsulin läßt sich nur in Bouin-fixiertem, nicht aber in Karnovsky-fixiertem Gewebe immunhistologisch nachweisen, während das Insulin des normalen Pankreas auch nach Karnovsky-Fixation immunhistologisch nachweisbar ist. Die Befunde sprechen für Unterschiede zwischen normalem pankreatischen und Tumor-Insulin. — Die Färbung der B-Zellen von Tumoren mit Aldehyd-Thionin gelingt seltener als der immunhistologische Nachweis von Insulin in diesen Zellen. Die immunhistologische Untersuchung ist daher zur Identifizierung von B-Zelltumoren den üblichen spezifischen Färbungen überlegen.
    Notes: Summary 14 insulinomas were examined immunohistologically using the peroxidase labelled antibody method. 8 tumours were investigated immediately after extirpation. 7 of these reacted with insulin and porcine-C-peptide antisera but not with glucagon antiserum. Only a B-cell carcinoma with an unusually low insulin concentration was negative. One year after embedding in paraffin the immunohistologic reaction with insulin antiserum had markedly decreased in the tumours; however, not in the islet of the adjacent pancreas. From 6 patients 1 to 4 years old paraffin-embedded material of the tumour and the normal pancreas was available. In this group 4 tumours with an elevated insulin concentration reacted immunohistologically only weakly with an insulin antiserum and two tumours (one with high and one with low insulin concentration were immunohistologically negative, while the islets of the adjacent panceas of all six cases showed a strong reaction. Thus the immunohistilogic reaction of insulin in B-cell tumours but not in normal islets depends on the time elapsed between the paraffin embedding and the examination. Only tumours fixed in Bouin's fluid but not in Karnovsky's solution gave a positive immunohistologie reaction, while the islets of the adjacent pancreas reacted positively also after fixation in Karnovsky's solution. These findings suggest differences between the normal and the tumour insulin. A correlation between aldehyde-thionin stain and immunohistology indicates the superiority of immunohistology in identifying insulin producing tumour cells.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: Insulinoma ; IRI content of insulinoma ; ultrastructural categorization of insulinomas ; proinsulin content of insulinomas ; functional defect in insulinomas reduced storage capacity of insulinoma cells ; non-granular insulin release ; proinsulin content of human pancreas ; diazoxide response of insulinomas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Thirty human insulinomas have been investigated histologically and their immunoreactive insulin (IRI) content estimated. In most cases immunohistological and ultrastructural studies were also performed and the percentage of proinsulin-like components (PLC) in the tumour determined. Except for 1 case the IRI concentration in the tumours was lower (0.01–89.0 U/g) than in the islet tissue. Histologically, immunohistologically and ultrastructurally a variable number of tumour cells contained few and often no beta-granules, indicating a decreased storage capacity for insulin. This defective storage capacity seems to be the major functional abnormality of insulinoma cells. Ultrastructurally four types of insulinoma can be distinguished. The ultra-structural diagnosis of an insulinoma can only be made in type I (typical beta-granules, 13 cases) and type II (typical and atypical granules, 7 cases) but not in type III (atypical granules only, 4 cases) and type IV (virtually agranular, 4 cases). The type IV tumours had the lowest IRI concentration and did not respond to diazoxide treatment. The IRI concentration of the uninvolved pancreas of 19 patients was 2.0±0.2 U/g and in the range of non-diabetic adults. — The percentage PLC in 19 insulinomas was higher (5.3–22%) than in the pancreas of human adults with and without insulinoma (1.7–4.8%). The percentage of PLC in the serum of patients with insulinoma was always higher than in their tumours (33–61%). It is suggested that the higher PLC levels found in the tumour and serum of insulinoma patients are the consequence of the reduced storage capacity of the tumour cells resulting in a rapid passage through the granular route or even a non-granular release of newly synthesized insulin.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0428
    Keywords: GIP ; gastrin ; insulin ; incretin ; chronic pancreatitis ; test meal ; malassimilation of fat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Twenty-nine patients with chronic pancreatitis had a significantly greater IR-GIP response to a test meal than 15 controls. This increased response was not related to the degree of steatorrhoea or glucose intolerance. It was most marked in a group of patients with moderately impaired IRI release and medium steatorrhoea. From this is concluded that the IR-GIP response to a test meal is determined by at least two factors: 1. feedback control via insulin secretion, 2. assimilation of fat. In chronic pancreatitis endocrine insufficiency may induce an exaggerated GIP response and severe exocrine insufficiency may prevent fat induced GIP release. Gastrin is not involved in the different GIP response in patients with chronic pancreatitis.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0428
    Keywords: GIP ; gastrin ; insulin ; incretin ; coeliac disease ; duodeno-pancreatectomy ; chronic pancreatitis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The response of serum immunoreactive gastric inhibitory polypeptide (IR-GIP), gastrin (IRG) and insulin (IRI) to a mixed standard meal was measured in 15 controls, 6 patients with coeliac disease, 26 patients with chronic pancreatitis and 6 patients with chronic pancreatitis and partial duodenopancreatectomy (Whipple's procedure). Serum levels of IR-GIP, IRG and IRI were significantly reduced in patients with coeliac disease. The serum glucose increase was significantly smaller only during the first hour after the meal. Since small intestinal GIP- and G-cells are situated mainly in the glands of duodenal and jejunal mucosa their absolute number is not significantly reduced in coeliac disease. It is suggested that the release of IR-GIP and duodenal IRG is influenced by the rate of absorption of nutrients. In patients with chronic pancreatitis the IR-GIP release is significantly greater than in controls, the IRG release normal and the IRI response delayed. After Whipple's procedure the IR-GIP response is increased significantly while the IRG secretion is abolished. This demonstrates that the duodenum is not necessary for GIP release and that pancreatic and jejunal gastrin are without clinical significance.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1573-2568
    Keywords: gastric acid ; secretion ; inhibition ; achlorhydria ; Helicobacter pylori ; gastritis ; atrophic gastritis ; pernicious anemia ; gastrin ; endocrine cells ; argyrophil cells ; carcinoid ; carcinoma ; tumors ; metaplasia ; dysplasia ; hyperplasia ; Zollinger-Ellison syndrome ; multiple endocrine neoplasia type I ; H2-receptor antagonists ; cimetidine ; ranitidine ; proton pump inhibitors ; omeprazole ; gastric surgery ; vagotomy ; gastrectomy ; nutrition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A critical evaluation has been made of the available evidence in man of the effects of prolonged low acid states on the structure and function of the stomach. Various human models have been examined. 1. Ageing does not affect acid output from the normal male stomach, and there may be an increase in women. With progressive atrophy of the corpus mucosa, which is more frequent and rapid in patients with gastric ulcer, there is an associated loss of secretory function. Chronic gastritis and atrophy are the most important age-related changes, which in many cultures are hypothesized to develop via a priorHelicobacter pylori-related gastritis. However,H. pylori colonization of the mucosa decreases with increasing grades of gastric atrophy probably because intestinal metaplasia provides a hostile environment. Atrophy and intestinal metaplasia are sociated with precancerous lesions and gastric cancer. Apparent hyperplasia of the gastric argyrophil endocrine cells is a common and spontaneous phenomenon in patients with atrophic gastritis, which in part may be related to the preferential loss of nonendocrine cells. 2. Pernicious anemia is associated with a complete lack of acid production, marked hypergastrinemia, and endocrine cell hyperplasia in the majority of patients. ECL-cell carcinoids and gastric cancer occur with a prevalence of 3–7%, and endoscopic surveillance in routine clinical practice is not warranted. 3. Gastric ECL-cell carcinoids are rare events that have been described in association with two diseases in man, pernicious anemia and Zollinger-Ellison syndrome as part of multiple presence of chronic atrophic gastritis with gastric antibodies or a genetic defect rather than the presence or absence of acid. Regression or disappearance of ECL-cell carcinoids, either spontaneously or after removal of the gastrin drive, has been recorded. Lymph node, and rarely hepatic, metastases are documented but death in these cases has been anecdotal. 4. Therapy with H2 antagonists may result in up to a twofold rise in serum gastrin levels but in man no endocrine cell hyperplasia has been recorded. However, the data for H2 antagonists on these aspects are very limited. There is no drug-related risk of gastric or esophageal cancer, although the incidence of the latter may be raised. Long-term treatment with omeprazole is associated with a two-to fourfold increase in gastrin levels over baseline values in one third of patients and apparent endocrine cell hyperplasia in 7% of cases overall. The endocrine cell hyperplasia is correlated with both levels of hypergastrinemia and the changes of progressive atrophic gastritis. No metaplastic, dysplastic, or neoplastic changes have been reported to date on long-term therapy with omeprazole. Monitoring patients on any form of long-term antisecretory therapy, for changes in serum gastrin or endoscopy with biopsy, is not recommended as part of routine clinical practice. Bacterial overgrowth in patients on any of the antisecretory drugs has not proven to be a problem clinically. 5. Gastric surgery may have profound effects on gastric function, depending on the type of operation. Hypergastrinemia, generally higher than that reported in patients on H2 antagonists or omeprazole, has been reported following all types of vagotomy. Endocrine cell changes have not been adequately studied. The issue of nitrosation and cancer risk remains hypothetical, dogged by methodological problems and conflicting results. Overall, the risk of gastric cancer after gastric resection does not become significant until 20–25 years later, and even then endoscopic screening is not justified. 6. The nutritional consequences of diseases and therapies in which there is a low acid state cannot easily be predicted but are only likely to occur over a very long time course, over 20 years in many reports. 7. The evidence for any increase in the occurrence of cancer at extragastric sites, such as pancreas or colon, in patients with prolonged low acid states is limited and conflicting. Overall, the risks of significant changes in gastric structure or function as a result of long-term low acid status in man have been over-stated and analogies with animal data have not been supported by the currently available evidence in humans.
    Type of Medium: Electronic Resource
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